It is the broad objective of this project to obtain a clearer understanding of the pathophysiology and biochemistry of alcoholic liver disease so that ultimately a more rational approach to therapy may be used. It has been well established that excess ethanol ingestion early results in an increased triglyceride accumulation in the liver (fatty liver). The responsible metabolite or combination of metabolites for this occurrence has never been established. Preliminary studies by the principal investigator suggest that both a lowered redox potential (NAD plus/NADH ratio) as well as increased acetate may play a significant role in the development of the acute alcoholic fatty liver. This project involves a comprehensive investigation to establish the character and mechanism of these hepatic lipid alterations seen after acute ethanol ingestion.